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Enhancement of UVB radiation–mediated apoptosis by sanguinarine in HaCaT human immortalized keratinocytes
Open accessAbstract
In this article, we studied the chemopreventive effects of sanguinarine on UVB-mediated responses in human HaCaT immortalized keratinocytes. For our studies, HaCaT cells were treated with a low dose (50 nmol/L) of sanguinarine for 24 hours followed by irradiation with UVB (15 or 30 mJ/cm2). Our data showed that UVB exposure, at both doses, resulted in decreased cell viability and increased apoptosis. Interestingly, pretreatment of the cells with sanguinarine caused a significant enhancement in the antiproliferative response of UVB. These responses on UVB and/or sanguinarine treatments were associated with (a) decrease in Bcl-2 and Bcl-XL and (b) increase in Bax, Bid, and Bak protein levels. Bax knockdown and Bcl-2 overexpression resulted in a rescue of HaCaT cells from sanguinarine-mediated apoptosis. DNA cell cycle analysis revealed that UVB treatment resulted in an accumulation of cells in the G2-M phase of the cell cycle, whereas pretreatment of sanguinarine resulted in a significant shift of cells in the S phase at a low UVB dose and a further accumulation of cells in the G2-M phase at a higher UVB dose. These effects on cell cycle were accompanied with modulations in the protein levels of cyclin (B1, E, and A) and cdc2 and cyclin-dependent kinase 1. Furthermore, sanguinarine treatment was found to result in significant modulations in p53, p66Shc, MsrA, and superoxide dismutase levels. Based on our data, we suggest the sanguinarine may protect skin cells from UVB-mediated damages via apoptotic elimination of damaged cells that escape programmed cell death and therefore possess a potential of clonal expansion. [Mol Cancer Ther 2006;5(2):418–29]
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Sanguinarine protected the cell from apoptosis via modulating the tumor suppressor protein p53 and pro-apoptotic BAX, BAK, BID and BCL-2 pathways.
“On the other hand, it protected the cell from apoptosis via modulating the tumor suppressor protein p53 and pro-apoptotic BAX (BCL-2-associated X protein), BAK (BCL-2 antagonist killer 1), BID (BCL-2-interacting domain death agonist) and BCL-2 (B-cell lymphoma-2) pathways (Reagan- Shaw et al. 2006).”
From Skin protection from solar ultraviolet radiation using natural compounds: a review (2024) · cites this paper as Reagan-Shaw et al. 2006
The Results section reports that sanguinarine pretreatment increased Bax, Bid, and Bak and decreased Bcl-2 in a pattern favoring apoptosis—not protection from it. The Discussion likewise says sanguinarine enhanced UVB-damaged HaCaT cells’ ability to undergo apoptosis. The paper describes protection from UVB damage through elimination of damaged cells, not protection of those cells from apoptosis. (LLM, conf=0.94)
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Experimental — accuracy not yet measuredIn an in vitro study, UV-B irradiation increased the number of human keratinocyte (HaCaT) cells in the gap 2-mitosis phase of the cell cycle, but pretreatment with sanguinarine dramatically shifted cells toward the synthesis phase.
“According to an in vitro study, UV-B irradiation increased the number of human keratinocyte (HaCaT) cells in the gap 2-mitosis phase of the cell cycle, but pretreatment with sanguinarine dramatically shifted cells toward the synthesis phase.”
From Skin protection from solar ultraviolet radiation using natural compounds: a review (2024) · cites this paper as Reagan-Shaw et al. 2006
The Discussion (page not supplied) says UVB caused G2–M arrest in HaCaT cells and sanguinarine pretreatment caused significant S-phase arrest at 15 mJ/cm² UVB. At 30 mJ/cm², however, pretreatment caused G2–M arrest instead, so the claimed shift toward S phase needs a low-dose qualifier. (LLM, conf=0.91)
Experimental — accuracy not yet measuredReagan-Shaw et al. obtained a significant decrease of SOD activity (MnSOD) after treatment with sanguinarine, enhancing UV-B-mediated oxidative stress in HaCaT cells.
“Reagan-Shaw et al. [5] have also obtained a significant decrease of SOD activity (MnSOD) after treatment with sanguinarine, enhancing UV-B-mediated oxidative stress in HaCaT cells.”
From The Effect of Lycopene Preexposure on UV‐B‐Irradiated Human Keratinocytes (2016) · cites this paper as [5]
Changes in the Bax/Bcl-2 ratio suggest a corresponding change in mitochondrial permeability to release apoptogenic molecules from the mitochondria to the cytosol.
“Changes in the Bax/Bcl-2 ratio suggest a corresponding change in mitochondrial permeability to release apoptogenic molecules from the mitochondria to the cytosol [5].”
From The Effect of Lycopene Preexposure on UV‐B‐Irradiated Human Keratinocytes (2016) · cites this paper as [5]
Cell cycle arrest increases the time available for DNA repair before its replication and mutation fixation processes.
“Cell cycle arrest increases the time available for DNA repair before its replication and mutation fixation processes [5].”
From The Effect of Lycopene Preexposure on UV‐B‐Irradiated Human Keratinocytes (2016) · cites this paper as [5]
Similar results were obtained by Reagan-Shaw et al. who suggested that sanguinarine may protect skin cells from UVB-mediated damage via apoptotic elimination of damaged cells that escaped from programmed cell death.
“In general, similar results were obtained by Reagan-Shaw et al. [5] who suggested that sanguinarine (also a botanical antioxidant) may protect skin cells (also HaCaT cell line) from UVB-mediated damage via apoptotic elimination of damaged cells that escaped from the programmed cell death.”
From The Effect of Lycopene Preexposure on UV‐B‐Irradiated Human Keratinocytes (2016) · cites this paper as [5]
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References 67 · Cited by 64
Metadata
- Authors
- Reagan-Shaw, S., Breur, J., & Ahmad, N.
- Affiliations
- 1Department of Dermatology,
- University of Wisconsin–Madison (US)
- ORCID
- Ahmad, Nihal
- Venue
- Molecular Cancer Therapeutics
- Published
- 2006-02-01
- Volume
- 5
- Issue
- 2
- Pages
- 418-429
- ISSN
- 1535-7163 (ISSN-L)
- 1538-8514
- OpenAlex
- W1963995610
- Cited by
- 64
- References
- 67
- Citations by year
- 2026: 1 · 2025: 1 · 2024: 3 · 2023: 3 · 2022: 2 · 2021: 1 · 2020: 2 · 2019: 2 · 2018: 3 · 2017: 4 · 2016: 4 · 2015: 5 · 2014: 4 · 2013: 5 · 2012: 3
- FWCI
- 5.67
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Locations
- Molecular Cancer Therapeutics (publishedVersion)
- PubMed (publishedVersion)
- Funders
- National Institutes of Health (5r03ca099076-02)
- National Cancer Institute (R03CA098368, CA099076, CA-098368)
- Topics
- Health Sciences › Medicine › Dermatology › Skin Protection and Aging
- Health Sciences › Medicine › Pharmacology (medical) › Berberine and alkaloids research
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Cancer Research › Photodynamic Therapy Research Studies
- Keywords
- sanguinarine, UV-B radiation, apoptosis, HaCaT keratinocytes, chemoprevention, Bcl-2 family proteins, Bax, cell cycle arrest, G2/M phase, cyclins, cdc2, p53, p66Shc, superoxide dismutase, skin cancer prevention, antiproliferative activity
- MeSH terms
- Src Homology 2 Domain-Containing, Transforming Protein 1, Alkaloids, Cell Cycle, Cell Line, Transformed, Colony-Forming Units Assay, Humans, Isoquinolines, Oxidoreductases, Radiation Tolerance, Radiation-Protective Agents, Superoxide Dismutase, Ultraviolet Rays, Down-Regulation, Keratinocytes, Up-Regulation, Tumor Suppressor Protein p53, Cyclins, Apoptosis, Oxidative Stress, Proto-Oncogene Proteins c-bcl-2, Adaptor Proteins, Signal Transducing, Methionine Sulfoxide Reductases, Benzophenanthridines, Shc Signaling Adaptor Proteins
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